Inhibition or enhancement of immunological injury of virus-infected cells.
Within hours after infection of cells with herpes simplex, vaccinia, influenza, or Newcastle disease virus, new antigens appeared on the surface of infected cells. The interaction of specific antiviral antibody and complement with these antigens resulted in cell destruction, which was quantitated by the release of (51)Cr. A number of factors can influence the degree of cell destruction, including the density of viral antigens on the surface of infected cells, the nature of the antiviral antibody, and the presence of anti-immunoglobulins. The immunological destruction of virus-infected cells may on the one hand serve as a defense mechanism against certain viral infections, while on the other hand it may contribute to the pathology of the host.
D000818:Animals; D000888:Antibodies, Anti-Idiotypic; D000918:Antibody Specificity; D000937:Antigen-Antibody Reactions; D000956:Antigens, Viral; D002460:Cell Line; D002470:Cell Survival; D002477:Cells / Q000276:immunology; D002478:Cells, Cultured; D002859:Chromium Isotopes; D003165:Complement System Proteins; D006041:Goats; D006367:HeLa Cells; D006561:Herpes Simplex / Q000276:immunology*; D006801:Humans; D007106:Immune Sera; D007251:Influenza, Human / Q000276:immunology*; D007668:Kidney; D008168:Lung; D009521:Newcastle Disease / Q000276:immunology*; D011200:Poultry; D011817:Rabbits; D013045:Species Specificity; D014615:Vaccinia / Q000276:immunology*
D000888:Antibodies, Anti-Idiotypic; D000956:Antigens, Viral; D002859:Chromium Isotopes; D007106:Immune Sera; D003165:Complement System Proteins